Baroreceptors are integral to cardiovascular control, primarily influencing heart rate, vascular tone, and cardiac output. The carotid sinus baroreceptors relay information through the carotid sinus nerve (the nerve of Hering), a branch of the glossopharyngeal nerve (cranial nerve IX), to the NTS. Simultaneously, baroreceptors in the aortic arch send signals through the aortic depressor nerve, which joins the vagus nerve (cranial nerve X). The signals ultimately converge in the NTS, which then adjusts sympathetic and parasympathetic activity to modulate blood pressure.
The baroreceptor reflex helps regulate systemic blood pressure by coordinating the autonomic response. When blood pressure rises, increased baroreceptor firing decreases sympathetic tone and increases parasympathetic activity, resulting in vasodilation and a reduction in cardiac output. The opposite occurs when blood pressure falls—sympathetic activity increases, causing vasoconstriction and boosting cardiac output to restore blood pressure.
The cardiopulmonary receptors are themselves low-pressure baroreceptors, located in the atria, the ventricles and the pulmonary vessels, and their afferents also travel in the vagus nerve to the NTS. They monitor filling rather than arterial pressure. Atrial stretch suppresses vasopressin release from the posterior pituitary, releases atrial natriuretic peptide and reduces renal sympathetic nerve activity, which lowers renin secretion, so a full circulation promotes a sodium and water diuresis. A fall in blood volume removes that inhibition: vasopressin, renin, angiotensin II and aldosterone rise, sympathetic outflow to the heart and kidney increases, heart rate and cardiac output are supported, and the kidney retains fluid to restore circulating volume. The low-pressure receptors therefore act on volume over hours to days, complementing the second-to-second arterial reflex.
Two named reflexes arise from these cardiac receptors and are easy to confuse because they produce opposite heart rate responses. The Bainbridge reflex is a response to atrial stretch: a rapid rise in venous return, such as a fast fluid bolus, stretches receptors at the venoatrial junctions and the heart rate rises (through vagal withdrawal with a sympathetic contribution) to move the extra volume forward. It is most evident when the resting heart rate is slow, and it is the reason the heart rate may climb during a rapid infusion in a well-filled patient. The Bezold-Jarisch reflex is the opposite pattern and arises mainly from the left ventricle: mechanoreceptors and chemoreceptors with unmyelinated vagal C-fiber afferents respond to a vigorously contracting, underfilled ventricle (or to chemical stimuli such as ischemic metabolites) with the triad of bradycardia, vasodilation and hypotension. It is the mechanism behind sudden bradycardia or asystole during spinal anesthesia when venous pooling empties the ventricle, during shoulder surgery in the sitting position (especially after epinephrine has reached the circulation from an interscalene block), with hemorrhage, and in inferior myocardial infarction. The treatment is restoration of preload with the legs raised and fluid, together with ephedrine, atropine or, when the bradycardia is profound or progressing, early small doses of epinephrine.
